Education/Training/Appointments

Laura Benjamin earned a Ph.D. in Molecular Biology from the University of Pennsylvania in 1995. She then performed her postdoctoral study at the Hebrew University-Hadassah Medical School with Eli Keshet. In 1999, Dr. Benjamin joined the Harvard Faculty as an Assistant Professor in the Department of Pathology at Beth Israel Deaconess Medical Center, and later became an Associate Professor in 2005. In 2008, Dr. Benjamin became the Associate Director of the Center for Vascular Biology Research.

Research Interests

Mechanisms of Blood and Lymphatic Angiogenesis

Basic Research

My research has focused on the study of molecular mechanisms that regulate vascular morphogenesis and function. My early work focused on the microvascular remodeling process in angiogenesis of both developmental and tumor vascular beds. This work highlighted the importance of VEGF as a survival factor for a remodeling vasculature and the role of pericytes in relieving VEGF dependence. More recent studies in my laboratory have focused on the role of important signaling pathways in the tumor vasculature and how regulation of those pathways contributes to tumor progression. In particular, our emphasis has been on the AKT pathway, which plays important roles in maintaining endothelial survival and governing microvascular permeability. We have ongoing projects on AKT regulation and the function of downstream signaling. We also have a real interest in exploring the impact of developing therapeutics in the tumor stroma with the notion that many of these rely on stromal responses as components of their efficacy. Going forward we are committing a significant portion of our energy to the study of the lymphatic vasculature from the perspective of novel regulatory pathways that control lymphangiogenesis to the role of lymphatic dysfunction in disease. We have identified novel molecular pathways that differentially impact vascular and lymphatic gene expression. In this context we are investigating lymphatic contributions to the pathologies associated with diabetes as well as cancer metastasis and response to cancer therapy.

Phung TL, Ziv K, Dabydeen D, Eyiah-Mensah G, Riveros M, Perruzzi C, Sun J-F, Monahan-Early R, Shiojima I, Nagy JA, Lin MI, Walsh K, Dvorak AM, Briscoe DM, Neeman M, Sessa WC, Dvorak HF,
Benjamin LE. Pathological angiogenesis is induced by sustained Akt signaling and inhibited by rapamycin. Cancer Cell. 2006
This manuscript described the consequences of sustained Akt signaling in the vasculature on both the structure and function of blood vessels. The main point in this study was that sustained signaling was capable of reproducing many of the abnormalities we associate with tumor blood vessels and that blocking this pathway induced structural and functional 'normalization' of those vessels.